Only a few risk factors that are clearly associated in adulthood with the development of premature atherosclerosis are identifiable in childhood, and their true ability to predict increased risk in the majority of children is uncertain. Studies of cholesterol homeostasis in adults have revealed individuals with an inability to precisely compensate for cholesterol in the diet by either decreasing cholesterol synthesis or cholesterol absorption, or increasing fecal cholesterol excretion. With new stable isotopic tracers of cholesterol and sitosterol, it is now possible to extend these studies to the first two years of life to determine if adult patterns of cholesterol homeostatis also occur in this young age group. Once the methods are developed to study infants and toddlers, a longitudinal study is planned of cholesterol homeostasis in infancy and of the feedback regulation of cholesterol homeostasis in response to changes in dietary cholesterol quantity and fat quality at age two. The results will increase the limited understanding of the consequences of dietary modifications of cholesterol and fat in early childhood, and of the metabolic dysfunctions underlying the pathogenesis of atherosclerosis.